Chemokines trigger immediate β2 integrin affinity and mobility changes:: Differential regulation and roles in lymphocyte arrest under flow
Chemokines trigger immediate β2 integrin affinity and mobility changes:: Differential regulation and roles in lymphocyte arrest under flow
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DOI：
10.1016/s1074-7613(00)00074-1
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发表时间：
2000-12-01
期刊：
影响因子：
32.4
通讯作者：
Laudanna, C
中科院分区：
文献类型：
--
作者：
Constantin, G;Majeed, M;Laudanna, C
趋化因子触发快速整合素依赖性淋巴细胞阻滞至血管内皮。我们发现趋化因子SLC、ELC和SDF-1 α可迅速诱导β 2整合素LFA-I的侧向迁移和亲和力的瞬时增加。抑制磷脂酰肌醇3-OH激酶（PI（3）K）的活性阻断流动性，但不是亲和力的变化，并防止淋巴细胞粘附到ICAM-1固定在低，但不是高密度，这表明流动性提高高亲和力整合素和配体之间的频率，但在较高的配体密度的亲和力变化是足够的逮捕。因此，趋化因子通过不同的信号传导途径触发LFA-1的高亲和力状态和侧向移动性，其可以在生理条件下协调地确定循环淋巴细胞的血管阻滞。
Chemokines trigger rapid integrin-dependent lymphocyte arrest to Vascular endothelium. We show that the chemokines SLC, ELC, and SDF-1 alpha rapidly induce lateral mobility and transient increase of affinity of the beta2 integrin LFA-I. Inhibition of phosphatidylinositol 3-OH kinase (PI(3)K) activity blocks mobility but not affinity changes and prevents lymphocyte adhesion to ICAM-1 immobilized at low but not high densities, suggesting that mobility enhances the frequency of encounters between high-affinity integrin and ligand but that at higher ligand density affinity changes are sufficient for arrest. Thus, chemokines trigger, through distinct signaling pathways, both a high-affinity state and lateral mobility of LFA-1 that can coordinately determine the vascular arrest of circulating lymphocytes under physiologic conditions.